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What Causes Kussmaul Respirations In Dka?

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetes mellitus is the name given to a group of conditions whose common hallmark is a raised blood glucose concentration (hyperglycemia) due to an absolute or relative deficiency of the pancreatic hormone insulin. In the UK there are 1.4 million registered diabetic patients, approximately 3 % of the population. In addition, an estimated 1 million remain undiagnosed. It is a growing health problem: In 1998, the World Health Organization (WHO) predicted a doubling of the worldwide prevalence of diabetes from 150 million to 300 million by 2025. For a very tiny minority, diabetes is a secondary feature of primary endocrine disease such as acromegaly (growth hormone excess) or Cushing’s syndrome (excess corticosteroid), and for these patients successful treatment of the primary disease cures diabetes. Most diabetic patients, however, are classified as suffering either type 1 or type 2 diabetes. Type 1 diabetes Type 1 diabetes, which accounts for around 15 % of the total diabetic population, is an autoimmune disease of the pancreas in which the insulin-producing β-cells of the pancreas are selectively destroyed, resulting in an absolute insulin deficiency. The condition arises in genetically susceptible individuals exposed to undefined environmental insult(s) (possibly viral infection) early in life. It usually becomes clinically evident and therefore diagnosed during late childhood, with peak incidence between 11 and 13 years of age, although the autoimmune-mediated β-cell destruction begins many years earlier. There is currently no cure and type 1 diabetics have an absolute life-long requirement for daily insulin injections to survive. Type 2 diabetes This is the most common form of diabetes: around 85 % of the diabetic population has type 2 diabetes. The primary prob Continue reading >>

Respiratory System And Diabetes

Respiratory System And Diabetes

Tweet The respiratory system is the system of organs that allow the body to take in oxygen and expel carbon dioxide, this process is known as gaseous exchange. We generally breathe between 12 and 20 times a minute. There are a number of complications of diabetes that can negatively affect our breathing. Parts of the respiratory system The following parts of the body make up the respiratory system: Mouth and nose Trachea (windpipe) Lungs Diaphragm How the respiratory system works Breathing is usually initiated by contraction of the diaphragm, a muscle which separates the chest cavity from the abdomen. Tweet Type 2 diabetes mellitus is a metabolic disorder that results in hyperglycemia (high blood glucose levels) due to the body: Being ineffective at using the insulin it has produced; also known as insulin resistance and/or Being unable to produce enough insulin Type 2 diabetes is characterised by the body being unable to metabolise glucose (a simple sugar). This leads to high levels of blood glucose which over time may damage the organs of the body. From this, it can be understood that for someone with diabetes something that is food for ordinary people can become a sort of metabolic poison. This is why people with diabetes are advised to avoid sources of dietary sugar. The good news is for very many people with type 2 diabetes this is all they have to do to stay well. If you can keep your blood sugar lower by avoiding dietary sugar, likely you will never need long-term medication. Type 2 diabetes was formerly known as non-insulin-dependent or adult-onset diabetes due to its occurrence mainly in people over 40. However, type 2 diabetes is now becoming more common in young adults, teens and children and accounts for roughly 90% of all diabetes cases worldwide. How serious Continue reading >>

(kussmaul's Breathing)

(kussmaul's Breathing)

De Raes EA, Benoit DD, … Decruyenaere JM CONCLUSIONS: Malignant lactic acidosis is a rare and often rapidly fatal metabolic complication if not promptly recognized and treated. An elevated lactic acid concentration, in disproportion with the level of tissue hypoxia, together with high serum LDH are cornerstones in the diagnosis. In contrast to septic shock patients, pronounced polypnea (Kussmaul's breathing pattern) rather than the haemodynamic instability is prominent. Continue reading >>

Diabetic Ketoacidosis And Hyperglycaemic Hyperosmolar State

Diabetic Ketoacidosis And Hyperglycaemic Hyperosmolar State

The hallmark of diabetes is a raised plasma glucose resulting from an absolute or relative lack of insulin action. Untreated, this can lead to two distinct yet overlapping life-threatening emergencies. Near-complete lack of insulin will result in diabetic ketoacidosis, which is therefore more characteristic of type 1 diabetes, whereas partial insulin deficiency will suppress hepatic ketogenesis but not hepatic glucose output, resulting in hyperglycaemia and dehydration, and culminating in the hyperglycaemic hyperosmolar state. Hyperglycaemia is characteristic of diabetic ketoacidosis, particularly in the previously undiagnosed, but it is the acidosis and the associated electrolyte disorders that make this a life-threatening condition. Hyperglycaemia is the dominant feature of the hyperglycaemic hyperosmolar state, causing severe polyuria and fluid loss and leading to cellular dehydration. Progression from uncontrolled diabetes to a metabolic emergency may result from unrecognised diabetes, sometimes aggravated by glucose containing drinks, or metabolic stress due to infection or intercurrent illness and associated with increased levels of counter-regulatory hormones. Since diabetic ketoacidosis and the hyperglycaemic hyperosmolar state have a similar underlying pathophysiology the principles of treatment are similar (but not identical), and the conditions may be considered two extremes of a spectrum of disease, with individual patients often showing aspects of both. Pathogenesis of DKA and HHS Insulin is a powerful anabolic hormone which helps nutrients to enter the cells, where these nutrients can be used either as fuel or as building blocks for cell growth and expansion. The complementary action of insulin is to antagonise the breakdown of fuel stores. Thus, the relea Continue reading >>

Kussmaul Breathing

Kussmaul Breathing

Not to be confused with Kussmaul's sign. Graph showing the Kussmaul breathing and other pathological breathing patterns. Kussmaul breathing is a deep and labored breathing pattern often associated with severe metabolic acidosis, particularly diabetic ketoacidosis (DKA) but also kidney failure. It is a form of hyperventilation, which is any breathing pattern that reduces carbon dioxide in the blood due to increased rate or depth of respiration. In metabolic acidosis, breathing is first rapid and shallow[1] but as acidosis worsens, breathing gradually becomes deep, labored and gasping. It is this latter type of breathing pattern that is referred to as Kussmaul breathing. Terminology[edit] Adolph Kussmaul, who introduced the term, referred to breathing when metabolic acidosis was sufficiently severe for the respiratory rate to be abnormal or reduced.[2] This definition is also followed by several other sources,[3][4] including for instance Merriam-Webster, which defines Kussmaul breathing as "abnormally slow deep respiration characteristic of air hunger and occurring especially in acidotic states".[5] Other sources, however, use the term Kussmaul respiration also when acidosis is less severe, in which case breathing is rapid.[4][6] Note that Kussmaul breathing occurs only in advanced stages of acidosis, and is fairly rarely reached. In less severe cases of acidosis, rapid, shallow breathing is seen. Kussmaul breathing is a kind of very deep, gasping, desperate breathing. Occasionally, medical literature refers to any abnormal breathing pattern in acidosis as Kussmaul breathing; however, this is inaccurate. History[edit] Kussmaul breathing is named for Adolph Kussmaul,[2] the 19th century German doctor who first noted it among patients with advanced diabetes mellitus. Kussm Continue reading >>

Acid-base Physiology

Acid-base Physiology

An outline of management is presented: this should be tailored to individual circumstances. Management of DKA has passed through 3 stages in the last 100 years: Stage 1: Preinsulin era (Feature: mortality of 100%) Stage 2: High dose insulin regime (Feature: mortality down to 10% but metabolic complications due to the treatment) Stage 3 (the present): Low dose insulin regime (Feature: low mortality) Mortality with the low dose insulin regime is down to about 2 to 5% overall. In older patients with DKA precipitated by a major medical illness (eg acute pancreatitis, myocardial infarction, septicaemia), the mortality rate is still high due to the severity of the precipitating problem. Restore normal carbohydrate and lipid metabolism Management can be considered in terms of emergency and routine components. Protect by intubation with a cuffed tube if patient is significantly obtunded. Consider placing a nasogastric tube in all patients. Intubation may be necessary for airway protection or ventilation (eg if aspiration, coma, pneumonia, pulmonary oedema, acute pancreatitis and ARDS) but this is not common. Maintain compensatory hyperventilation in intubated patients Patients with metabolic acidosis (eg severe DKA) have marked hyperventilation (ie respiratory compensation, Kussmaul respirations) and typically low arterial pCO2 levels. If intubated and ventilated, ventilatory parameters (tidal volume and rate) need to be set to continue a high minute ventilation. If this is not done and pCO2 is inappropriately high, a severe acidaemia and consequent severe cardiovascular collapse may occur This is a particular problem in all situations where a patient with a compensated metabolic acidosis is intubated and ventilated. The rule of thumb is to aim for a pCO2 level of 1.5 times th Continue reading >>

Ketoacidosis In Cats – Causes, Symptoms & Treatment

Ketoacidosis In Cats – Causes, Symptoms & Treatment

Ketoacidosis in cats at a glance Ketoacidosis is a serious complication of diabetes in which ketones and blood sugar levels build up in the body due to insufficient levels of insulin which is required to move glucose into the cells for energy. As a result, the body uses fat as an alternate energy source which produces ketones causing the blood to become too acidic. Common causes include uncontrolled diabetes, missed or insufficient insulin, surgery, infection, stress and obesity. Symptoms of ketoacidosis include increased urination and thirst, dehydration, nausea, diarrhea, confusion, rapid breathing which may later change to laboured breathing. What is diabetic ketoacidosis? Diabetic ketoacidosis (DKA) is a life-threatening complication of diabetes characterised by metabolic acidosis (increased acids in the blood), hyperglycemia (high blood glucose) and ketonuria (ketones in the urine). It is caused by a lack of or insufficient amounts of insulin which is required to move glucose from the bloodstream and into the cells to be used for energy. When this occurs, the body begins to search for alternate sources of energy and begins to break down fat. When fat is broken down (metabolised) into fatty acids, waste products known as ketones (acetoacetate, beta-hydroxybutyrate, acetone) are released from the liver and accumulate in the bloodstream (known as ketonemia). This causes the blood to become too acidic (metabolic acidosis). As well as metabolic acidosis, ketones also cause central nervous depression.The body will try to get rid of the ketones by excreting them out of the body via the urine, increased urine output leads to dehydration, making the problem worse. Meanwhile, the unused glucose remains in the bloodstream, resulting in hyperglycemia (high blood sugar).Insulin Continue reading >>

Diabetic Ketoacidosis (dka)

Diabetic Ketoacidosis (dka)

Learning Objectives 1.Diagnosis of DKA 2.Precipitants of DKA 3.Managment of DKA 4. LADA- late onset autoimm. diabetes of adulthood DKA is most common in DM1 but can occur in DM2 when under significant stress. Normally, insulin allows tissue (mostly muscle) to take up glucose and suppresses lipolysis and proteolysis (anabolic state) When under stress and with insulin deficiency, the body produces glucagon-> glycogenolysis-> hi blood glucose and increases lipolysis-> FFA like beta hydroxybutyrate and acetoactone which cause acidosis(catabolic state) Lab abnormalities: hi bg (blood glucose), agap acidosis, ketonemia, ketonuria "serum ketone" tests measure acetoacetone, which is just one of the 2 major ketones serum b- hydroxybutyrate is a more accurate test of ketonemia but less readily available ketonuria can have false positive with some drugs ie) captopril K+ may be high in serum due to acidemia causing extracellular shifts, but pt have overall low K+ BUN and creatinine may reflect dehydration as glucosuria causes osmotic diuresis PE: fruity breath (acetone), kussmaul's respirations (deep labored), tachycardia, hypotension Triggers: Infection ie) influenza, pneumonia, gastroenterits Significant stressors: ACS, CVA, drugs (cocaine, meth) Noncompliance: insulin pump dysfunction, insulin noncompliance Will Daines gave us a nice tool: "6 i's"causing dka infection, ischemia, insulin deficiency, intra-abd processes (compromising pancreatic function), iatrogenic (ie) steroids), and ingestions (meth, cocaine) Management of DKA 1.Confirm diagnosis (plasma glucose, positive serum ketones, metabolic acidosis). 2.Admit to hospital; ICU may be necessary for frequent monitoring or if pH < 7.00 or AMS 3.Assess: Serum electrolytes (K+, Na+, Mg2+, Cl-, bicarbonate, phosphate) Acid-base Continue reading >>

Diabetic Ketoacidosis (dka)

Diabetic Ketoacidosis (dka)

A 12 year old boy, previously healthy, is admitted to the hospital after 2 days of polyuria, polyphagia, nausea, vomiting and abdominal pain. Vital signs are: Temp 37C, BP 103/63 mmHg, HR 112, RR 30. Physical exam shows a lethargic boy. Labs are notable forWBC 16,000,Glucose 534, K 5.9, pH 7.13, PCO2 is 20 mmHg, PO2 is 90 mmHg. result of insulin, glucagon, growth hormone, catecholamine increased tidal volume and rate as a result of metabolic acidosis due to gluconeogenesis and glycogenolysis tissues unable to use the high glucose as it is unable to enter cells anion gap due to ketoacidosis, lactic acidosis consumed in an attempt to buffer the increased acid glucose acts as an osmotic agent and draws water from ICF to ECF acidosis results in ICF/ECF exchange of H+ for K+ depletion of total body potassium due to cellular shift and losses through urine -hydroxybutyrate not detected with normal ketone body tests due to in capillary lipoprotein lipase activity H2PO4- is increased in urine, as it is titratable acid used to buffer the excess H+ that is being excreted must prevent resultant hypokalemia and hypophosphatemia labs may show pseudo-hyperkalemia prior to administartion of fluid and insulin due to transcellular shift of potassium out of the cells to balance the H+ being transfered into the cells Upon administration of insulin, potassium will shift intracellularly, possibly resulting in dangerous hypokalemia give phosphatesupplementation to prevent respiratory paralysis (M1.EC.31) A 17-year-old male presents to your office complaining of polyuria, polydipsia, and unintentional weight loss of 12 pounds over the past 3 months. On physical examination, the patient is tachypneic with labored breathing. Which of the following electrolyte abnormalities would you most likely Continue reading >>

What Causes Diabetic Ketoacidosis? Symptoms & Complications

What Causes Diabetic Ketoacidosis? Symptoms & Complications

Risk factors for diabetic ketoacidosis are type 1 diabetes , and missing insulin doses frequently, or being exposed to a stressor requiring higher insulin doses ( infection , etc). Diabetic ketoacidosis is diagnosed by an elevated blood sugar ( glucose ) level, elevated blood ketones and acidity of the blood ( acidosis ). The treatment for diabetic ketoacidosis is insulin, fluids and electrolyte therapy . Diabetic ketoacidosis can be prevented by taking insulin as prescribed and monitoring glucose and ketone levels. The prognosis for a person with diabetic ketoacidosis depends on the severity of the disease and the other underlying medical conditions. Diabetic ketoacidosis (DKA) is a severe and life-threatening complication of diabetes . Diabetic ketoacidosis occurs when the cells in our body do not receive the sugar (glucose) they need for energy. This happens while there is plenty of glucose in the bloodstream, but not enough insulin to help convert glucose for use in the cells. The body recognizes this and starts breaking down muscle and fat for energy. This breakdown produces ketones (also called fatty acids ), which cause an imbalance in our electrolyte system leading to the ketoacidosis (a metabolic acidosis). The sugar that cannot be used because of the lack of insulin stays in the bloodstream (rather than going into the cell and provide energy). The kidneys filter some of the glucose (sugar) and excrete it in the urine . In general diabetic ketoacidosis occurs because there is not enough insulin to move sugar (glucose) into the cell where it can be used for energy. Besides lack of insulin, certain body stressors combined with diabetes , such as infection or illness, can trigger diabetic ketoacidosis. Sometimes diabetic ketoacidosis is the first sign of diabetes Continue reading >>

Abnormal Breathing Patterns

Abnormal Breathing Patterns

Apnea Absence of breathing. (Ap-knee-a) Eupnea Normal breathing (Eup-knee-a) Orthopnea Only able to breathe comfortable in upright position (such as sitting in chair), unable to breath laying down, (Or-thop-knee-a) Dyspnea Subjective sensation related by patient as to breathing difficulty Paroxysmal nocturnal dyspnea - attacks of severe shortness of breath that wakes a person from sleep, such that they have to sit up to catch their breath - common in patient's with congestive heart failure. Hyperpnea Increased volume with or without and increased frequency (RR), normal blood gases present. Hyperventilation "Over" ventilation - ventilation in excess of the body's need for CO2 elimination. Results in a decreased PaCO2, and a respiratory alkalosis. Hypoventilation "Under" ventilation - ventilation that is less than needed for CO2 elimination, and inadequate to maintain normal PaCO2. Results in respiratory acidosis. Can be a slow rate with normal tidal volumes such that the total minute ventilation is inadequate. Can be a normal rate but with such low tidal volumes that air exchange is only in the dead space and not effective. Tachypnea Increased frequency without blood gas abnormality Kussmaul's Respiration Kussmaul's respiration. Increased rate and depth of breathing over a prolonged period of time. In response to metabolic acidosis, the body's attempt to blow off CO2 to buffer a fixed acid such as ketones. Ketoacidosis is seen in diabetics. Cheyne-Stokes respirations (CSR) Gradual increase in volume and frequency, followed by a gradual decrease in volume and frequency, with apnea periods of 10 - 30 seconds between cycle. Described as a crescendo - decrescendo pattern. Characterized by cyclic waxing and waning ventilation with apnea gradually giving way to hyperpneic brea Continue reading >>

Pulmcrit- Dominating The Acidosis In Dka

Pulmcrit- Dominating The Acidosis In Dka

Management of acidosis in DKA is an ongoing source of confusion. There isn’t much high-quality evidence, nor will there ever be (1). However, a clear understanding of the physiology of DKA may help us treat this rationally and effectively. Physiology of ketoacidosis in DKA Ketoacidosis occurs due to an imbalance between insulin dose and insulin requirement: Many factors affect the insulin requirement: Individuals differ in their baseline insulin resistance and insulin requirements. Physiologic stress (e.g. hypovolemia, inflammation) increases the level of catecholamines and cortisol, which increases insulin resistance. Hyperglycemia and metabolic acidosis themselves increase insulin resistance (Souto 2011, Gosmanov 2014). DKA treatment generally consists of two phases: first, we must manage the ketoacidosis. Later, we must prepare the patient to transition back to their home insulin regimen. During both phases, success depends on balancing insulin dose and insulin requirement. Phase I (Take-off): Initial management of the DKA patient with worrisome acidosis Let’s start by considering a patient who presents in severe DKA with worrisome acidosis. This is uncommon. Features that might provoke worry include the following: bicarbonate < 7 mEq/L pH < 7 (if measured; there is generally little benefit from measuring pH) clinically ill-appearing (e.g., dyspnea, marked Kussmaul respirations) These patients generally have severe metabolic acidosis with respiratory compensation. This creates two concerns: If the metabolic acidosis worsens, they may decompensate. The patient is depending on respiratory compensation to maintain their pH. If they should fatigue and lose the ability to hyperventilate, their pH would drop. It is important to reverse the acidosis before the patient m Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Practice Essentials Diabetic ketoacidosis (DKA) is an acute, major, life-threatening complication of diabetes that mainly occurs in patients with type 1 diabetes, but it is not uncommon in some patients with type 2 diabetes. This condition is a complex disordered metabolic state characterized by hyperglycemia, ketoacidosis, and ketonuria. Signs and symptoms The most common early symptoms of DKA are the insidious increase in polydipsia and polyuria. The following are other signs and symptoms of DKA: Nausea and vomiting; may be associated with diffuse abdominal pain, decreased appetite, and anorexia History of failure to comply with insulin therapy or missed insulin injections due to vomiting or psychological reasons or history of mechanical failure of insulin infusion pump Altered consciousness (eg, mild disorientation, confusion); frank coma is uncommon but may occur when the condition is neglected or with severe dehydration/acidosis Signs and symptoms of DKA associated with possible intercurrent infection are as follows: See Clinical Presentation for more detail. Diagnosis On examination, general findings of DKA may include the following: Characteristic acetone (ketotic) breath odor In addition, evaluate patients for signs of possible intercurrent illnesses such as MI, UTI, pneumonia, and perinephric abscess. Search for signs of infection is mandatory in all cases. Testing Initial and repeat laboratory studies for patients with DKA include the following: Serum electrolyte levels (eg, potassium, sodium, chloride, magnesium, calcium, phosphorus) Note that high serum glucose levels may lead to dilutional hyponatremia; high triglyceride levels may lead to factitious low glucose levels; and high levels of ketone bodies may lead to factitious elevation of creatinine levels. Continue reading >>

Diabetic Ketoacidosis And Patho

Diabetic Ketoacidosis And Patho

pathophysiology ketogenesis due to insulin deficiency leads to increased serum levels of ketones anad ketonuria acetoacetate, beta-hydroxybutyrate; ketone bodies produced by the liver, organic acids that cause metabolic acidosis respiration partially compensates; reduces pCO2, when pH < 7.2, deep rapid respirations (Kussmaul breathing) acetone; minor product of ketogenesis, can smell fruity on breath of ketoacidosis patients elevated anion gap Methanol intoxication Uremic acidosis Diabetic ketoacidosis Paraldehyde ingestions Intoxicants (salicyclate, ethylene glycol, nipride, epinephrine, norepinephrine) Lactic acidosis (drug induced; didanosine, iron, isoniazid, metformin, zidovudine) Ethanol ketoacidosis Severe renal failure starvation Blood glucose regulation (6) 1. When blood glucose levels rise above a set point, 2. the pancreas secretes insulin into the blood. 3. Insulin stimulates liver and muscle cells to make glycogen, dropping blood glucose levels. 4. When glucose levels drop below a set point, 5. the pancreas secretes glucagon into the blood. 6. Glucagon promotes the breakdown of glycogen and the release of glucose into the blood. (The pancreas signals distant cells to regulate levels in the blood = endocrine function.) Insulin and Glucagon (Regulation) (10) 1. High blood glucose 2. Beta cells 3. Insulin 4. Glucose enters cell 5. Blood glucose lowered 6. Low blood glucose 7. Alpha cells 8. Glucagon 9. Liver releases glucose from glycogen 10. Blood glucose raised What is the manifestations (symptoms) of Type 1? (10) 1. Extreme thirst 2. Frequent urination 3. Drowsiness, lethargy 4. Sugar in urine 5. Sudden vision change 6. Increased appetite 7. Sudden weight loss 8. Fruity, sweet, or wine like odor on breath 9. Heavy, laboured breathing 10. Stupor, unconscious Continue reading >>

Hyperglycaemic Crises And Lactic Acidosis In Diabetes Mellitus

Hyperglycaemic Crises And Lactic Acidosis In Diabetes Mellitus

Hyperglycaemic crises are discussed together followed by a separate section on lactic acidosis. DIABETIC KETOACIDOSIS (DKA) AND HYPERGLYCAEMIC HYPEROSMOLAR STATE (HHS) Definitions DKA has no universally agreed definition. Alberti proposed the working definition of “severe uncontrolled diabetes requiring emergency treatment with insulin and intravenous fluids and with a blood ketone body concentration of >5 mmol/l”.1 Given the limited availability of blood ketone body assays, a more pragmatic definition comprising a metabolic acidosis (pH <7.3), plasma bicarbonate <15 mmol/l, plasma glucose >13.9 mmol/l, and urine ketostix reaction ++ or plasma ketostix ⩾ + may be more workable in clinical practice.2 Classifying the severity of diabetic ketoacidosis is desirable, since it may assist in determining the management and monitoring of the patient. Such a classification is based on the severity of acidosis (table 1). A caveat to this approach is that the presence of an intercurrent illness, that may not necessarily affect the level of acidosis, may markedly affect outcome: a recent study showed that the two most important factors predicting mortality in DKA were severe intercurrent illness and pH <7.0.3 HHS replaces the older terms, “hyperglycaemic hyperosmolar non-ketotic coma” and “hyperglycaemic hyperosmolar non-ketotic state”, because alterations of sensoria may be present without coma, and mild to moderate ketosis is commonly present in this state.4,5 Definitions vary according to the degree of hyperglycaemia and elevation of osmolality required. Table 1 summarises the definition of Kitabchi et al.5 Epidemiology The annual incidence of DKA among subjects with type 1 diabetes is between 1% and 5% in European and American series6–10 and this incidence appear Continue reading >>

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